IL18 Antibody - #DF6252

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製品: IL18 Antibody
カタログ: DF6252
タンパク質の説明: Rabbit polyclonal antibody to IL18
アプリケーション: WB IHC IF/ICC
反応性: Human, Mouse, Rat
分子量: 22kDa; 22kD(Calculated).
ユニプロット: Q14116
RRID: AB_2838218

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WB Handbook
IHC Protocol
IF/ICC Protocol

製品説明

ソース:
Rabbit
アプリケーション:
WB 1:500-1:2000, IHC 1:50-1:200, IF/ICC 1:100-1:500
*The optimal dilutions should be determined by the end user.
*Tips:

WB: For western blot detection of denatured protein samples. IHC: For immunohistochemical detection of paraffin sections (IHC-p) or frozen sections (IHC-f) of tissue samples. IF/ICC: For immunofluorescence detection of cell samples. ELISA(peptide): For ELISA detection of antigenic peptide.

反応性:
Human,Mouse,Rat
クローナリティ:
Polyclonal
特異性:
IL18 Antibody detects endogenous levels of total IL18.
RRID:
AB_2838218
引用形式: Affinity Biosciences Cat# DF6252, RRID:AB_2838218.
コンジュゲート:
Unconjugated.
精製:
The antiserum was purified by peptide affinity chromatography using SulfoLink™ Coupling Resin (Thermo Fisher Scientific).
保存:
Rabbit IgG in phosphate buffered saline , pH 7.4, 150mM NaCl, 0.02% sodium azide and 50% glycerol. Store at -20 °C. Stable for 12 months from date of receipt.
別名:

折りたたみ／展開

Iboctadekin; IFN gamma inducing factor; IFN-gamma-inducing factor; IGIF; IL 1 gamma; IL 18; IL 1g; IL-1 gamma; IL-18; IL1 gamma; IL18; IL18 protein; IL18_HUMAN; IL1F4; IL1g; IL1gamma; ILIF4; Interferon gamma inducing factor; Interferon gamma-inducing factor; Interleukin 1 gamma; Interleukin 18 (interferon-gamma-inducing factor); Interleukin 18; Interleukin-1 gamma; Interleukin-18; Interleukin18; MGC12320;

免疫原

免疫原:
Uniprot:

Q14116(IL18_HUMAN) >>Visit HPA database.

遺伝子(ID):
IL18(3606)
タンパク質の説明:
The protein encoded by this gene is a proinflammatory cytokine that augments natural killer cell activity in spleen cells, and stimulates interferon gamma production in T-helper type I cells. Alternatively spliced transcript variants encoding different isoforms have been found for this gene.[provided by RefSeq, Aug 2011]
タンパク質配列:
MAAEPVEDNCINFVAMKFIDNTLYFIAEDDENLESDYFGKLESKLSVIRNLNDQVLFIDQGNRPLFEDMTDSDCRDNAPRTIFIISMYKDSQPRGMAVTISVKCEKISTLSCENKIISFKEMNPPDNIKDTKSDIIFFQRSVPGHDNKMQFESSSYEGYFLACEKERDLFKLILKKEDELGDRSIMFTVQNED

PTMs - Q14116 基板として

Site PTM Type Enzyme
Y37 Phosphorylation
Y88 Phosphorylation
K106 Ubiquitination
K115 Acetylation
K115 Ubiquitination
K120 Acetylation
K120 Ubiquitination
K132 Ubiquitination
S133 Phosphorylation
K171 Ubiquitination

研究背景

機能:

A proinflammatory cytokine primarily involved in polarized T-helper 1 (Th1) cell and natural killer (NK) cell immune responses (Probable). Upon binding to IL18R1 and IL18RAP, forms a signaling ternary complex which activates NF-kappa-B, triggering synthesis of inflammatory mediators. Synergizes with IL12/interleukin-12 to induce IFNG synthesis from T-helper 1 (Th1) cells and natural killer (NK) cells (Probable).

PTMs:

The pro-IL-18 precursor is processed by CASP1 or CASP4 to yield the active form.

細胞の位置付け:

Secreted.

Extracellular region or secreted Cytosol Plasma membrane Cytoskeleton Lysosome Endosome Peroxisome ER Golgi apparatus Nucleus Mitochondrion Manual annotation Automatic computational assertionSubcellular location
サブユニット構造:

Forms a ternary complex with ligand-binding receptor subunit IL18R1 and signaling receptor subunit IL18RAP at the plasma membrane. Mature IL18 first binds to IL18R1 forming a low affinity binary complex, which then interacts with IL18RAP to form a high affinity ternary complex that signals inside the cell.

タンパク質ファミリー:

Belongs to the IL-1 family.

研究領域

· Environmental Information Processing > Signaling molecules and interaction > Cytokine-cytokine receptor interaction.   (View pathway)

· Human Diseases > Infectious diseases: Bacterial > Salmonella infection.

· Human Diseases > Infectious diseases: Bacterial > Legionellosis.

· Human Diseases > Infectious diseases: Parasitic > African trypanosomiasis.

· Human Diseases > Infectious diseases: Parasitic > Malaria.

· Human Diseases > Infectious diseases: Bacterial > Tuberculosis.

· Human Diseases > Infectious diseases: Viral > Influenza A.

· Human Diseases > Immune diseases > Inflammatory bowel disease (IBD).

· Human Diseases > Immune diseases > Rheumatoid arthritis.

· Organismal Systems > Immune system > NOD-like receptor signaling pathway.   (View pathway)

· Organismal Systems > Immune system > Cytosolic DNA-sensing pathway.   (View pathway)

参考文献

1). Overexpression of NAG-1/GDF15 prevents hepatic steatosis through inhibiting oxidative stress-mediated dsDNA release and AIM2 inflammasome activation. Redox Biology, 2022 (PubMed: 35504134) [IF=10.7]
2). Identification of circulating T-cell immunoglobulin and mucin domain 4 as a potential biomarker for coronary heart disease. MedComm, 2023 (PubMed: 37426678) [IF=9.9]

Application: WB    Species: Mouse    Sample: RAW264.7 cells

FIGURE 3 Ox‐LDL increased ADAM17 and sTIMD4 while decreased mTIMD4 level in macrophages. RAW264.7 cells were treated with ox‐LDL at the indicated concentrations for 24 h (A, D–G) or with 80 μg/mL ox‐LDL for the indicated times (B) or LPS at 1 μg/mL for 24 h (C). After treatment, total cellular proteins, RNA, and treatment mediums were collected. (A–C) Expression of ADAM17, mTIMD4, IL‐6, IL‐10, pro‐IL‐1β, IL‐1β, caspase‐1, and IL‐18 in cells and sTIMD4 in medium was detected by Western blotting (n = 3). (D and E) Expression of TIMD4, ADAM17, TNF‐α, and IL‐6 mRNA was determined by qRT‐PCR (n = 3–4). HSP90 was used as a loading control. *p < 0.05; **p < 0.01; ns, not significant.
3). Betulinic Acid Inhibits ROS-Mediated Pyroptosis in Spinal Cord Injury by Augmenting Autophagy via the AMPK-mTOR-TFEB Signaling Pathway. International Journal of Biological Sciences, 2020 (PubMed: 33867836) [IF=8.2]

Application: WB    Species: Mice    Sample: spinal cords

Figure 2 BA attenuates pyroptosis after SCI. (A) Immunofluorescence staining for Caspase-1 and NeuN co-localization in the spinal cords of the Sham, SCI, and BA groups (scale bar = 25 µm) (B) The quantitative mean optical density of the Caspase-1 in motor neurons of spinal cord lesion. (C) Immunofluorescence staining for GSDMD and NeuN co-localization in the spinal cords of the Sham, SCI, and BA groups (scale bar = 25 µm) (D) The quantitative mean optical density of the GSDMD in motor neurons of spinal cord lesion. (E)Western blotting for ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels in the Sham, SCI, and BA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (F) The optical density values of the ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels were quantified and analyzed in each group. The values are expressed as the means ± SEM, n=5 per group. **p< 0.01, vs. Sham group. #p< 0.05 and ##p< 0.01, vs. SCI group.

Application: WB    Species: Mice    Sample: spinal cords

Figure 2 BA attenuates pyroptosis after SCI. (A) Immunofluorescence staining for Caspase-1 and NeuN co-localization in the spinal cords of the Sham, SCI, and BA groups (scale bar = 25 µm) (B) The quantitative mean optical density of the Caspase-1 in motor neurons of spinal cord lesion. (C) Immunofluorescence staining for GSDMD and NeuN co-localization in the spinal cords of the Sham, SCI, and BA groups (scale bar = 25 µm) (D) The quantitative mean optical density of the GSDMD in motor neurons of spinal cord lesion. (E)Western blotting for ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels in the Sham, SCI, and BA groups. The gels were run under the same experimental conditions, and the cropped blots are shown here. (F) The optical density values of the ASC, Caspase-1, GSDMD, IL-1β, IL-18 and NLRP3 expression levels were quantified and analyzed in each group. The values are expressed as the means ± SEM, n=5 per group. **p< 0.01, vs. Sham group. #p< 0.05 and ##p< 0.01, vs. SCI group.
4). Myoglobin promotes macrophage polarization to M1 type and pyroptosis via the RIG-I/Caspase1/GSDMD signaling pathway in CS-AKI. Cell Death Discovery, 2022 (PubMed: 35228524) [IF=7.0]
5). Protective role of hydrogen sulfide against diabetic cardiomyopathy by inhibiting pyroptosis and myocardial fibrosis. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2024 (PubMed: 38657502) [IF=6.9]
6). Biliverdin modulates the Nrf2/A20/eEF1A2 axis to alleviate cerebral ischemia-reperfusion injury by inhibiting pyroptosis. Biomedicine & Pharmacotherapy, 2023 (PubMed: 37399716) [IF=6.9]

Application: WB    Species: Mouse    Sample:

Fig. 2. Biliverdin can alleviate CIRI by inhibiting pyroptosis in mice. A. NLRP3, ASC, GSDMD-N, and β-actin western blot images; B. Cleaved-Caspase-1, IL-1β, IL-18, and β-actin western blot images; C. Expression of NLRP3; D. ASC expression; E. GSDMD-N expression; F. Cleaved-Caspase-1 expression; G. IL-1β expression; H. IL-18 expression. According to Sham group，
7). 1,8-cineole ameliorates experimental diabetic angiopathy by inhibiting NLRP3 inflammasome-mediated pyroptosis in HUVECs via SIRT2. Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie, 2024 (PubMed: 38972150) [IF=6.9]

Application: WB    Species: Mouse    Sample:

Fig. 2. 1,8-cineole decreases the expression of pyroptosis-related proteins in the thoracic aorta of DM mice. (A, B) Expression of the protein SIRT2 associated with pyroptosis in the thoracic aorta of diabetic mice was assessed using western blotting. (C, D) Effect of 1,8-cineole on the levels of IL-18 and IL-1β in murine serum. (E) Effect of 1,8-cineole on the concentration of lactate dehydrogenase (LDH) in mouse serum. Results are presented as the mean ± SD (n = 6), *p < 0.05, **p < 0.01 versus control group; #p < 0.05, ##p < 0.01 versus DM group.
8). The gut microbiota attenuate neuroinflammation in manganese exposure by inhibiting cerebral NLRP3 inflammasome. BIOMEDICINE & PHARMACOTHERAPY, 2020 (PubMed: 32768944) [IF=6.9]

Application: WB    Species: Rat    Sample: brain tissue

Fig. 4. Effect of Mn exposure and FMT on the brain-associated profile of NLRP3 inflammasome and inflammatory factors. (a–e) The activation level of NLRP3 inflammasome and inflammatory factors in the brain of rats. After FMT from healthy rats, the expression of IL-1β, IL-18, NLRP3, and TLR4 in brain was significantly downregulated, which were significantly different from that in Mn-treated group. *P < 0.05, **P < 0.01, ***P < 0.001.
9). A snake cathelicidin enhances transcription factor EB-mediated autophagy and alleviates ROS-induced pyroptosis after ischaemia-reperfusion injury of island skin flaps. British journal of pharmacology, 2024 (PubMed: 37850255) [IF=6.8]
10). Cyclic helix B peptide promotes random‐pattern skin flap survival via TFE3‐mediated enhancement of autophagy and reduction of ROS levels. British Journal of Pharmacology, 2022 (PubMed: 34622942) [IF=6.8]

Application: WB    Species: Mouse    Sample: skin tissues

FIGURE 3 CHBP inhibits pyroptosis in random-pattern skin flaps. (a–d) Skin tissue sections were stained with anti-GSDMD-N (green) or anti-caspase 1 (CASP1; red) immunofluorescence antibodies (DAPI staining of the nuclei). Scale bar: 10 μm. The number of positive cells is shown on the right of representative images (n = 6 mice per group). (e,f) CHBP treatment reduced the expression of NLRP3, ASC, caspase 1 (CASP1), GSDMD-N, IL-1β and IL-18 in the context of ischaemia–reperfusion injury. Densitometric quantification is shown on the right (n = 6 mice per group). (g–j) CHBP treatment attenuated the activation of GSDMD, IL-1β, IL-18 and caspase 1 in the skin tissues detected by ELISA kits (n = 6 mice per group). Data shown are means ± SEM. *P 
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